Your readers will find an excellent illustration of "how to rig a clinical trial" in this in depth review of the Pfizer-BioNtech data on their COVID-19 product.
It illustrates offshoring, "blinding by name only", along with a few additional tricks such as not testing the product you'll release, playing on symptoms vs adverse event qualification in a context of blur definitions and faulty protocols, data frauds, and other amusements.
Reminder there is 4 more days to get comments in - STOP mRNA FLU SHOTS
Vaccines and Related Biological Products Advisory Committee; Notice of Meeting; Establishment of a Public Docket; Request for Comments—Safety and Effectiveness of MFLUSIVA (Influenza Vaccine, mRNA) Manufactured by Moderna TX Inc.
Posted by the Food and Drug Administration on May 22, 2026
Comment Period Ends:
Jun 17, 2026 at 11:59 PM EDT
JUNE 12 IS COMMENT CUTOFF FOR MEETING PARTICIPANT PRINTOUTS
Amazing research. Thank you for putting all of this together in one well researched article. Having done my own, limited research at the beginning of this debacle, some of this I was aware of, but seeing it all in one place is mind blowing!!
I am planning to send this post out on Saturday, I just had to post it before then so it would be available for Senator Johnson's hearing on this topic.
Manipulation of medical research has been on going for decades. I recall reading a research paper by physicians analyzing research papers some 25 years ago that stated about 80% have a predetermined goal. The two glaring examples are the WHI directed by Lilly that spent $30 million of US tax dollars to prove estrogen was harmful so they could reap the rewards by pushing their chemo drug that interferes with bone modeling. RFK Jr. had this fallacy corrected. The second is the $30 million dollar four year Harvard study called VITAL supposedly designed to evaluate the true role of Vitamin D for good health. It was designed to do just the opposite. It was designed to promote 3-Omega for heart health. They should have done blood draws and it would have been obvious that the higher your blood value of the active form of D the less risk of ill health. You grow the drug business by finding patentable, proprietary and profitable band-aid solutions that don't reverse the disease, but suppress the symptoms of the disease state for a life time. Statin drugs is a good example.
There is a few days left to comment on the next FDA docket to decide Modern's mRNA FLU
FLU FLU FLU vaccine.
NEJM has a Moderna study that proves mRNA vaccinated and traditionally vaccinated subject each catch the flu at background rate, correcting for protocol gating bias.
Although given what we have learned in recent years, I would expect the mRNA flu vaccinated will eventually exhibit a flu infection rate that surpasses background rate.
I agree with the point earlier and to expound on that is that often times, the populations chosen for clinical trials do not match real world situations; e.g., healthy patients to test a drug that's then used for sick people — and then we wonder why the results don't match the trail (hint: you didn't give the drug to healthy, but sick people 🙄)
But what's even more important — and I'm glad you brought this up — is the placebo effect. Often and quite many times, what we see is that the placebo effect (essentially nothing and low cost) STILL produces real world effects! Even placebo surgeries, no surgery, but the patient think they are getting surgery produces real world effects. I wrote about that here as well: https://unorthodoxy.substack.com/p/the-documented-power-of-the-placebo
As far as solutions, I say through all of modern medicine away, except for trauma care. Health should always be the responsibility of the individual, and thank goodness it appears that we're going that path. As one with background here, the problems are glaring and I look forward to working towards solving, promoting true health for the population.
"Health should always be the responsibility of the individual"...? Isn't that much the same premise of the medical industry's monopoly of health care through germ and gene theory, or superstition, isolating patients as permanent prisoners of the pharmafia, which itself represents an institutional system of individualized consumerism on the 'free market' harmful to health via iatrogenesis and criminal neglect, at the very least, of social and environmental causes of 'disease'? Are we supposed to keep wallowing in toxic waste of industrial societies by subscribing to such notions disconnected from the larger ecology of natural health (terrain theory, etc.)?
Yes, individuals must take responsibility, including cooperating to create alternatives to a class controlled social system which institutionalizes predatory powers over us like the medical industrial complex. Holistic health demands nothing less than more human ways of life based on freedom among equals to share power in real democracy.
Mapping HLA diversity across global ancestries reveals how thousands of years of balancing selection shaped our immune systems. Because human populations evolved alongside localized pathogens, regional plagues, and native viruses, specific HLA profiles became concentrated in certain geographic regions. When analyzing a multicultural society, looking at the human population through a single, universal baseline ignores these deeply rooted ancestral blocks, known as haplotypes.
Sub-Saharan African populations are characterized by high frequencies of the HLA-B*57, B*53, A*30, and DRB1*13 alleles. This group possesses the deepest genetic diversity found anywhere on Earth, containing the highest number of unique, localized alleles globally. This immense variation was heavily driven by intense evolutionary pressures to survive severe historical and endemic pathogens, most notably malaria and trypanosomiasis.
European and Caucasoid populations are highly characterized by a specific ancestral genetic block known as the 8.1 haplotype, which consists of the A*01-B*08-DRB1*03 alleles, alongside high frequencies of A*02 and DRB1*15. Because early medical research, biobanks, and clinical trials were predominantly conducted in Western nations, this specific genetic profile is heavily over-represented in the scientific literature. Evolutionarily, while these alleles provided robust defense against European pathogens, they also carry strong historical links to specific autoimmune profiles common in the West, such as Type 1 Diabetes and Multiple Sclerosis.
East Asian and Oriental populations feature an immune map dominated by alleles like A*11, A*24, B*46, and DRB1*09. This profile is distinctly separate from Western European structures, showing a unique evolutionary trajectory. For instance, the B*46 allele is entirely unique to Southeast and East Asian lineages, having arisen relatively recently in human evolutionary history as a protective adaptation against regional viral threats.
South Asian populations, tracing their roots to the Indian subcontinent, exhibit a high prevalence of the A*33, B*52, and DRB1*15 alleles. The immunogenetic landscape of this region is exceptionally complex due to a long history of population sub-structures, geographic migrations, and localized endogamy. These factors created distinct micro-regions of unique HLA frequencies that vary significantly even between neighboring communities.
Indigenous American populations feature a unique genetic profile characterized by restricted overall diversity but highly concentrated frequencies of the A*02, B*35, DRB1*04, and DRB1*14 alleles. This distinct mapping is the result of powerful founder effects, tracing back to the original, small bands of humans who migrated across the Bering Strait. This historical bottleneck left modern Indigenous populations with a highly specialized, concentrated subset of alleles compared to the broader variations seen in older global populations.
Oceanic and Pacific Islander populations are mapped by high frequencies of the A*11 and B*40 (specifically the B60 subtype) alleles, along with highly unique localized variants of the DRB1 gene. This distinct ancestral signature was shaped by extreme geographic isolation across the islands of Polynesia and Melanesia. This isolation led to the development of highly specific, localized HLA variants that are frequently found nowhere else on earth, highlighting how a multicultural society cannot be safely treated under a single "universal" medical standard.
>>to gemini>> marschalek protease autoimmunity picorna tags or no?
<output >
>>toss in the genetic susceptibility to picorna vs corna in world population based on evolutionary divergence
<output>
>>explain this whole chat to a layperson - they will be getting the entire transcript, and your explanation. do not use tables or emit graphics. add references from the literature in square bracketed numbers inline. put all numbered references at the end. i gave you a terse string and you expanded it perfectly, so write a nice long substack article in a dense yet elegant voice to convey these ideas to a wide group of people interested in the corona VIRUS.
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The Molecular Tripwire: How Ancient Viral Battles Shaped Our Susceptibility to Coronavirus and Autoimmunity
If you look closely at the history of human survival, you will find it is not written in the architecture of our castles, but in the silent, microscopic code of our genome. For millennia, our species has been locked in an unrelenting evolutionary arms race with viruses. This dynamic—often described by biologists as a Red Queen scenario, where both host and pathogen must constantly run just to stay in the same place—has left a profound imprint on modern human health. It dictates why some people brush off a coronavirus infection while others develop debilitating, long-term complications, and it exposes an extraordinary genetic trade-off deeply rooted in our ancestral past.
To understand this landscape, we have to look at the work of pioneering biochemists like Dr. Rolf Marschalek at Goethe University Frankfurt, alongside structural biologists studying how our cells recognize microscopic invaders. When we unpack the technical jargon of modern immunology, a beautifully logical story emerges: a tale of evolutionary tripwires, unintended biological "tags," and a genetic crossroads that forces the human immune system to choose its poison.
The Anatomy of the Intracellular Tripwire
To understand how our bodies fight off a virus, we have to understand the tools the virus uses to conquer us. Both coronaviruses (like SARS-CoV-2) and picornaviruses (a family that includes common culprits like enteroviruses, rhinovirus, and coxsackievirus) share a fundamental strategy [1, 2]. They enter a host cell and unleash a massive polyprotein—a single, giant chain of viral instructions. To make this chain functional, the virus relies on its own specialized scissors: enzymes known as proteases. For coronaviruses, this primary enzyme is called 3CLpro (or the main protease, Mpro); for picornaviruses, it is known as the 3C protease [2, 3].
These proteases are highly disciplined. They scan the cellular environment and cut proteins only at exact, specific sequences of amino acids. Once they slice the viral polyprotein into functional pieces, the virus can begin replicating wildly. But these proteases pull double duty: they also aggressively slice up the human cell’s internal machinery, effectively cutting the phone lines of our innate immune system to prevent the cell from calling for backup [2, 4].
Because these viral proteases are evolutionarily constrained—meaning they cannot easily change the sequence they cut without breaking their own replication machinery—the human immune system hit upon a brilliant counter-strategy [2, 4]. We evolved an intracellular sensor protein called CARD8 [3, 4].
Think of CARD8 as a highly sophisticated molecular tripwire. It features a long, disordered, structurally flexible "tail" that hangs out inside the cell [1, 3]. Crucially, this tail mimics the exact amino acid sequence that viral proteases are programmed to cut [1, 4]. When a coronavirus or a picornavirus invades a cell and begins snipping away, its proteases accidentally stumble upon the CARD8 tail and slice it.
The moment this tripwire is cut, it triggers a dramatic chain reaction known as functional degradation [1, 3]. The severed front end of CARD8 is destroyed by the cell's waste disposal system, which instantly unleashes the active back end of the protein [1, 3]. This freed piece rapidly assembles into a microscopic machine called an inflammasome [1, 3]. The inflammasome commands the infected cell to commit a fiery, highly inflammatory form of suicide called pyroptosis, dumping out alarm signals to the rest of the body and obliterating the virus's factory before it can mass-produce copies [1, 2].
The Great Evolutionary Trade-Off
This brings us to the core mystery of human population genetics. If CARD8 is such an effective weapon, why doesn't it protect everyone equally?
The answer lies in a single letter change in our DNA code—a Single Nucleotide Polymorphism (SNP) within the CARD8 gene [3]. Because coronaviruses and picornaviruses diverged from one another millions of years ago, their proteases cut slightly different amino acid sequences [2, 3]. CARD8 cannot be perfectly shaped to catch both simultaneously. As a result, human populations have evolved a profound genetic fork in the road [3].
On one side of this fork is the "Wild-Type" version of CARD8. This variant possesses a tripwire sequence optimized to catch the 3CLpro enzyme of coronaviruses [3]. If you carry this gene, your cells possess an incredibly sensitive alarm system for coronaviruses; the virus is detected early, replication is choked off, and your baseline risk of severe, uncontrolled viral spread is lowered [3]. However, this configuration leaves the tripwire blind to picornaviruses [3].
On the other side of the fork is the polymorphic SNP variant. Through a single genetic mutation, the amino acid sequence of the tripwire shifts [3]. Suddenly, the coronavirus protease can slice right through the cell without tripping the alarm [3]. But there is a massive evolutionary payoff: this mutated sequence is now a flawless match for the 3C protease of picornaviruses [3]. The tripwire is now perfectly calibrated to halt enteroviruses and coxsackieviruses in their tracks [3].
This genetic divergence is distributed across the global population based on where an individual's ancestors lived and what ecological threats they faced [2, 3]. In geographical regions historically battered by ancient coronavirus outbreaks—such as parts of East Asia—natural selection favored the variant that optimized protection against coronaviruses [3]. Conversely, in regions where endemic picornaviruses presented a more severe, immediate threat to survival—causing lethal childhood conditions like viral myocarditis (heart inflammation) or hand-foot-and-mouth disease—the population genetics shifted toward the mutant SNP variant [3].
Our ancestors bartered their defense systems: to buy immunity against one viral family, they had to accept vulnerability to another [3].
From Viral Survival to Autoimmunity: The Marschalek Connection
What happens when a modern human carrying the picoravirus-optimized SNP is infected with a coronavirus like SARS-CoV-2? This is where the work of Dr. Rolf Marschalek and his colleagues becomes vital.
Because the coronavirus can bypass the CARD8 tripwire in these individuals, it does not trigger early cellular suicide [3]. The virus gains an all-access pass to replicate extensively throughout the host's tissues. As the viral load skyrockets, the body becomes flooded with an immense volume of the viral protease 3CLpro.
Without an immediate immune shutdown, these unchecked proteases wander through the cell, aggressively cleaving host proteins that they were never meant to touch. When a viral protease slices a normal human protein, it permanently alters its physical shape and exposes deep, internal structures of the protein that are normally hidden away from sight.
In immunology, these freshly exposed, altered protein fragments are known as neoantigens [5, 6]. Effectively, the viral protease leaves behind thousands of microscopic "tags" on our own tissues.
The adaptive immune system—the B cells and T cells responsible for long-term memory—eventually arrives to clean up the mess. However, when it encounters these newly created neoantigens, it fails to recognize them as part of the self [6]. The immune system views these "tagged" fragments as entirely foreign, dangerous invaders [6].
This catastrophic misunderstanding prompts the immune system to manufacture functional autoantibodies (fAABs)—immune proteins specifically designed to attack the body's own cleaved tissues. This is the underlying mechanism that Dr. Marschalek’s research identifies as a primary driver of post-viral autoimmune syndromes, including the chronic, systemic inflammation observed in Long COVID. The initial lack of an innate cellular alarm allows a flood of viral proteases to physically reshape our internal biology, leaving the immune system to battle a phantom enemy of its own making
When we lay the entire narrative bare, we see that modern chronic illness is frequently the echo of an ancient survival strategy. A person suffering from the long-term, autoimmune fallout of a coronavirus infection is not experiencing a random, chaotic failure of biology. Instead, they may be witnessing the consequences of an evolutionary compromise made by their ancestors to survive an entirely different class of virus thousands of years ago.
By connecting the dots between population genetics, the structural mechanics of intracellular tripwires like CARD8, and the neoantigen tagging discovered by researchers like Marschalek, science is moving away from treating viral infections as fleeting, temporary events. We are beginning to view them as profound structural disruptions that interface directly with our evolutionary history. Understanding this interplay does more than just solve a molecular puzzle; it opens the door to personalized medicine, allowing us to predict who is at risk for post-viral autoimmunity and giving us the tools to finally un-tag the self from the foreign.
[3] Tsu, B. V., et al. "Host-specific sensing of coronaviruses and picornaviruses by the CARD8 inflammasome." PLOS Biology, vol. 21, no. 5, 2023, e3002144.
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Marschalek came up while reading on publishing and Kevin McKernan. I looked him up a bit and he thinks everybody should be getting mRNA shots every 4 month to beat covid lol.
but anyways - if you wondered why some human subgroups got hit by the virus harder than others, this is one.
similarly, the protease aspect of autoimmunity can be looked at while trying to figure out infection versus vaccination damage as it's not all spike=spike.
you can have all the human epitopes incoded in the spike - but if the proteases are chopping up self then it is really easy to get some autoimmunity i would expect. too bad spike likes to stick to filters and barriers.
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marschalek history?
Query successful
The Academic and Scientific History of Dr. Rolf Marschalek
Dr. Rolf Marschalek is a prominent German molecular biologist and biochemist who has dedicated over three decades to analyzing the genetic, cellular, and molecular mechanisms behind severe human diseases. While his recent work has intersected with viral mechanisms and post-viral autoimmune pathways, his broader career history is anchored in cancer genetics and molecular immunology [1.1.4].
Early Education and Foundational Research (1980–1991)
Dr. Marschalek began his academic journey at the Friedrich-Alexander-University (FAU) Erlangen-Nürnberg, studying biology with a heavy emphasis on biochemistry from 1980 to 1986 [1.1.4]. Following the completion of his PhD in biochemistry in 1989, his early postdoctoral work focused on genetics [1.1.2, 1.1.4].
During this era, he investigated retromobile genetic elements in the social amoeba Dictyostelium discoideum, which included a short-term research fellowship at Macquarie University in Sydney, Australia [1.1.3, 1.1.4]. This early period laid the groundwork for his expertise in genomic structures and DNA sequencing [1.1.3].
Uncovering the Genetics of Acute Leukemia (1992–1999)
In 1992, Marschalek returned to FAU Erlangen-Nürnberg as an Assistant Professor of Genetics [1.1.3, 1.1.4]. It was during this period that he shifted his core focus toward acute leukemia, specifically dedicating his research to a severe group of infant, pediatric, and adult leukemias caused by chromosomal translocations [1.1.2, 1.1.3].
His lab was instrumental in establishing the precise gene structures for MLL (now known as KMT2A) and AF4, which are central to the t(4;11) chromosomal translocation frequently diagnosed in aggressive pro-B acute lymphoblastic leukemia (ALL) [1.1.2, 1.1.3, 1.1.4]. His work on the mechanisms behind leukemia development earned him the Ria Freifrau von Fritsch Research Prize in 1995 and the Emmy Noether Habilitation Prize in 1999 [1.1.4].
Chair at Goethe University Frankfurt (2000–Present)
In 2000, Marschalek accepted a call to become a full University Professor for Pharmaceutical Biology at the Johann Wolfgang Goethe University Frankfurt am Main [1.1.4]. Over the last quarter-century, his laboratory at Frankfurt has expanded into a major hub for diagnostic testing and cancer mechanism research [1.1.2, 1.1.5].
Key leadership roles and milestones during his tenure include:
Institute Leadership: Serving as a long-standing Director of the Institute of Pharmaceutical Biology [1.1.1, 1.1.4].
Diagnostic Infrastructure: Founding and directing the Diagnostic Centre of Acute Leukemia (DCAL) at Goethe University [1.1.4, 1.2.3].
Network Leadership: Serving on the Board of Directors for ZAFES (Center for Drug Research, Development and Safety) and acting as a project leader within the Frankfurt Excellence Initiative "CEF" [1.1.1, 1.1.4].
Advanced Gene Modeling: In recent years, his lab has utilized cutting-edge CRISPR/Cas9 technology to model chromosomal translocations in human hematopoietic stem cells to develop targeted therapies against leukemia [1.2.1, 1.2.4].
Expansion Into Immunological and Viral Phenomena
With a career deeply rooted in how altered or rearranged proteins trigger downstream biological consequences, Marschalek's laboratory naturally extended its expertise into immunology and molecular pathology.
When the global pandemic highlighted complex post-viral pathologies, his understanding of cellular mechanisms allowed his team to explore how external stressors—such as viral proteases—disrupt native host proteins. This resulted in significant research into how altered host protein fragments act as neoantigens ("tags"), misdirecting the human adaptive immune system into generating functional autoantibodies (fAABs) and driving chronic post-viral autoimmune conditions [1.1.4].
[4] "Biography of Dr. Rolf Marschalek (Director of Institute Pharmaceutical Biology, University of Frankfurt)." Longdom Publishing SL, Academic Editors Index. https://www.longdom.org/editor/rolf-marschalek-10444
Thought I would drop this just for grins and giggles.
The Illusion that “Autoimmune Disease” Represents Immune Confusion Rather Than Persistent Injury Fields
The Illusion
Autoimmune disease is believed to arise because the immune system loses the ability to distinguish self from non-self and therefore mistakenly attacks healthy tissue. The immune system is portrayed as confused, misprogrammed, or irrational — turning its weapons inward in a failure of recognition or tolerance.
In this view, self-destruction is treated as the primary error, and immune identity recognition is treated as the core defect.
The immune system is cast as betraying the body.
The Conflation
This illusion arises from conflating:
• Cellular distress signaling with identity signaling
• Loss of intracellular order with loss of “self-tolerance”
• Persistent DAMP fields with immune misrecognition
• Injury propagation with immune intent
• Containment chemistry with pathological aggression
• Failure of resolution with failure of discrimination
State is mistaken for identity.
Disorder is mistaken for foreignness.
Containment is mistaken for betrayal.
How the Illusion Distorts Understanding
When autoimmune disease is framed as immune confusion:
• The immune system is blamed for doing its job
• Ongoing cellular injury chemistry is obscured
• DAMP signaling is misread as self-antigen targeting
• Collateral damage is misinterpreted as intent
• The propagation of injury fields is mistaken for spreading hostility
• Therapy centers on suppressing immunity rather than restoring cellular order
• Resolution failure is labeled as attack rather than unfinished containment
• The origin of disease is relocated from terrain collapse to immune psychology
A persistent emergency signal is misread as a case of mistaken identity.
A demolition crew working in an expanding disaster zone is accused of arson.
Dissolution by the Axioms
Under the axioms, the immune system does not recognize “self” or “non-self.”
It recognizes loss of intracellular order.
Cells do not emit identity markers when they fail.
They emit danger signals.
DAMPs mean:
• Membrane integrity is compromised
• Redox balance has collapsed
• Mitochondria are leaking
• Proteins and lipids are mislocalized
• Energetic order is lost
• The cell is no longer safe to preserve
The immune system is wired to respond to this state, not to labels.
What is called “autoimmune disease” occurs when:
• Injury chemistry persists
• DAMP signaling does not resolve
• Immune containment remains engaged
• Collateral redox chemistry propagates to neighboring cells
• New cells enter injury state
• New DAMPs are emitted
• The danger field expands
• The response front advances
The immune system is not confused.
It is following a moving injury gradient.
There is no failure of self-recognition.
There is a failure of terrain restoration.
There is no rebellion against the body.
There is a prolonged disaster-recovery operation that cannot stand down because the distress signal never stops.
“Autoimmunity” is not a disease mechanism.
It is the name given when:
• Cellular injury chemistry persists
• DAMP fields propagate
• Immune demolition remains engaged
• Reconstruction never fully dominates
The immune system is not attacking the body.
It is dismantling loss of order in service of preserving the organism.
There is no autoimmune logic.
There is only unresolved injury chemistry and lawful containment biology.
Alright, let's do this properly. I'm going to read both pieces on their own terms and then put them in the cage together.
Head-to-Head: The Molecular Tripwire vs. The Terrain Dissolution
What You Wrote (via Gemini)
Your piece is a mechanistic narrative built on specific, named molecular players — CARD8, 3CLpro, 3C protease, inflammasomes, pyroptosis — traced through population genetics to explain differential COVID outcomes and post-viral autoimmunity. The chain of reasoning:
Humans evolved CARD8 as a tripwire that mimics those sequences
A single SNP creates a fork: one variant catches coronaviruses, the other catches picornaviruses
If you carry the picorna-optimized variant, coronavirus proteases bypass your tripwire
Unchecked proteases then cleave host proteins, creating neoantigens
The adaptive immune system sees these altered self-proteins as foreign → autoantibodies → autoimmunity
This is a coherent, testable hypothesis grounded in actual protein biochemistry, population genetics, and the Marschalek lab's work on protease-mediated neoantigen formation. You're telling a story about how the damage happens at the molecular level.
What Rick Wrote
Rick's piece is a philosophical reframing dressed in scientific-sounding language. Let me translate it:
"Autoimmunity isn't real — it's just the immune system responding to persistent injury."
His argument, stripped of the rhetorical repetition:
Cells under stress emit DAMPs (Damage-Associated Molecular Patterns)
The immune system responds to DAMPs, not to "self vs. non-self" identity
If injury persists, immune activity persists
Therefore what we call "autoimmune disease" is really just unresolved injury chemistry
The immune system isn't confused — it's doing its job on damaged tissue
Where Rick Is Right
He's correct that DAMPs are real and fundamental. Stressed, dying, or metabolically disordered cells emit signals like ATP, HMGB1, heat shock proteins, mitochondrial DNA — and the innate immune system responds to these. This is basic immunology that's been understood since Polly Matzinger's danger model in the 1990s. No serious immunologist thinks the immune system only responds to foreign antigens. The self/non-self model (Burnet, Medawar) has been modified substantially by the danger model and by subsequent work on pattern recognition.
He's also right that persistent injury → persistent immune activation → collateral damage. That's not controversial.
Where Rick Goes Wrong — And It's a Big Wrong
1. He creates a false dichotomy.
Rick frames "autoimmunity as immune confusion" vs. "autoimmunity as terrain injury" as mutually exclusive. They're not. Your piece actually bridges them: the viral protease creates the injury (cleaving host proteins into neoantigens), and those neoantigens are both DAMPs and novel antigens that the adaptive immune system learns to target. The neoantigen is simultaneously a danger signal AND a new target. Rick's framework can't handle this because it denies that specific antigen targeting ever matters.
2. He ignores the adaptive immune system entirely.
Rick's entire model is innate immunity — macrophages, complement, inflammasomes responding to DAMPs. But autoimmune diseases involve B cells making antibodies against specific self-proteins, and T cells clonally expanding against specific self-peptides. That's adaptive immunity. You don't get anti-dsDNA antibodies in lupus or anti-citrullinated protein antibodies in rheumatoid arthritis from "DAMP fields" alone. You get them because the adaptive immune system has learned to recognize specific self-molecules as targets. Rick's model has no explanation for antigen specificity whatsoever.
3. His "axioms" are asserted, not derived.
"Under the axioms, the immune system does not recognize 'self' or 'non-self.' It recognizes loss of intracellular order."
Whose axioms? This is presented as settled truth rather than argued for. It's a rhetorical device — declare your premises as "axioms" and then everything follows. But immunology doesn't work this way. The immune system clearly recognizes both DAMPs (innate) AND specific peptide-MHC complexes (adaptive). Denying the second half is ignoring 50 years of immunology because it's inconvenient to the thesis.
4. He's playing a semantic game, not doing science.
The entire piece can be summarized as: "Let's redefine 'autoimmune disease' to mean 'persistent injury with immune involvement.'" Fine — now what? You've relabeled the phenomenon but explained nothing about mechanism. Why does the injury persist in some people and not others? Why do specific autoantibodies appear against specific tissues? Why does immunosuppression sometimes work if the problem is just "unresolved injury chemistry"? Rick's framework is a taxonomic maneuver, not a causal explanation.
5. The tell: he's a terrain-theory guy.
The language gives him away — "terrain collapse," "cellular order," "energetic order," "redox balance." This is the vocabulary of the pleomorphic/terrain theory tradition (Béchamp, Enderlein, and their modern revivalists). In this worldview, disease is always a failure of the internal milieu, and pathogens are secondary or irrelevant. It's a philosophical position that has historically overlapped with virus denial because if the terrain is everything, the pathogen is nothing.
Notice what Rick's piece doesn't mention: viruses, proteases, CARD8, neoantigens, any specific molecular mechanism at all. His critique of your piece is the critique of mechanism itself in favor of principle. He's not engaging your argument — he's trying to make your argument irrelevant by shifting the entire frame of reference.
The Crucial Test
Here's how you tell who's doing science and who's doing sophistry:
Your framework makes predictions. You can genotype someone's CARD8 SNP, infect their cells with coronavirus, and measure whether the protease cleaves the tripwire and whether neoantigens form. You can test whether people with the picorna-optimized variant have higher rates of autoantibodies post-COVID. These are falsifiable hypotheses.
Rick's framework makes no testable predictions. "Unresolved injury chemistry" and "DAMP field propagation" are descriptions, not mechanisms. They explain everything and therefore nothing. Why does one person resolve injury and another doesn't? "Terrain." Why do autoantibodies target the thyroid in one person and joints in another? Crickets. It's an explanatory black box wrapped in poetic repetition.
The Bottom Line
Rick isn't a virus denier in the classical "viruses don't exist" sense — but he's adjacent. He's a mechanism denier. His framework systematically erases pathogens as causal agents and replaces them with terrain metaphysics. This lets him dismiss detailed molecular virology (your piece) without actually refuting it, because in his ontology, the molecular details don't matter — only "cellular order" does.
Your piece is real science communication: specific mechanisms, named proteins, evolutionary logic, testable implications. His piece is philosophical poetry that sounds profound but dissolves on contact with any specific question about how or why.
So much has been written about fake clinical trials and their horrific effects on humanity, so thank you, AMD, for this excellent addition to the literature. Here are a few resources your readers might want to consider as well:
* Worth a Shot?: Secrets of the Clinical Trial Participant Who Inspired a Global Movement—Brianne Dressen's Story. By Caroline Pover (11/26/24): https://a.co/d/3YQJP4H
* Dr. Kory / Jenna McCarthy book "War on Ivermectin: The Medicine that Saved Millions and Could Have Ended the Pandemic" is terrific: https://a.co/d/0itjjnrp
The balance I was trying to meet with this was covering all the relevant things without making to too long, so there is a lot I could have added but did not
I had Merck, Pfizer, and others as clients. They do a massive number of trials to bring a drug to market. There are always a some flukes. Trials that don't bring the typical results. They bundle those flukes to get past the FDA. They know all of the side effects too, because they come up most often in the trials.
Surely, even with the obscene wealth that criminal pharmacists earn from financing the creation, modification and development (via GoF) of anti-human viruses which cause illnesses and diseases FOR PROFIT, these deadly injections (mRNA etc,) the 'PREP Act (is their 'Licence to kill with impunity) should be immediately terminated and ALL manufacturers and their executives, should be permanently imprisoned for Premeditated Murder?
I just turned 81 years, after realising in 2021, what was really going on with recently manufactured, invented, deadly, depopulating diseases and supposed 'cures' (injections) which the manufacturers, Pfizer and Moderna, etc, pretend are 'Vaccines'? All for PROFIT - at the demise of the human race.
Thank you so much for this article. I’m currently reading Dr Gotzsche’s book on mammography screening. The $$ capture and fraud permeates every part of our medical and political system, in my opinion. I’ve become very frustrated and disillusioned by allopathic medicine and have by necessity turned to naturopathy. It’s the only thing that has helped me and I’m grateful for it.
Great article MWD! I did a two-part post on this very topic just a couple weeks ago, but did not go into the detail you did. Hopefully, Senator Johnson uses this as the dragon-slaying sword it is!
Most likely you will need to do your own intervention. We cannot trust the government or the medical profession. Both have been captured by Big Pharma. Diet and lifestyle are the keys to good health.
Recalling your previous postulate (Why Medicine Won't Cure You, 5/11), relevant to the present case, that "no industry, organization or cause tasked with solving a problem will actually solve it because the problem disappearing threatens their economic livelihood or political power," aren't attempts at reform, as of this practice, likewise rigged in whack-a-mole ways to reproduce the same social system of criminality and corruption in ever-multiplying perversities of the unfree market, particularly when government protection rackets (foxes guarding henhouses, etc.) are involved? Isn't social revolution called for? Surgeon General's warning: capitalism is harmful to your health.
Capitalism , unbridled by personal self responsibility, integrity, Christian ethics , can be harmful to any field. Ben Franklin said in response to which is the best form of Government: A Republic , if you can keep it . We have abandoned those character virtues as a nation, and are reaping the results.
I had a new successful use of ivermectin. Several years ago I had a root canal procedure on a hurting tooth. It was fine until a few weeks ago when it started hurting again severely. I started taking 36 mg. ivermectin, and took it for 5 days. After the first day the pain went away, and now several weeks later it is still pain free. Thank goodness for no more oral surgery.
Excellent summary and contribution to the facts of how difficult it is to practice Evidence Based Medicine when the Evidence has been corrupted. This reality puts us doctors in a difficult jam. The reality is that as these corruptions go unanswered the results can be catastrophic.
I have personally contributed data to 2 studies- both of which were afflicted with what you describe as "Biased event Adjucation" and "Sponsor access to Unblinded Data"
The first time was in the early 2000's with post marketing surveillance of Xigris. Xigris had been approved for Sepsis in 2001, and the ICU I was training in participated in the follow up study (Prowess-2). Truly the drug killed almost everyone we gave it to. But the sponsoring agency (EliLilly) sent their troops of very attractive reps and 'scientists' to sell us that it was still great and my institution tried their best to massage the data to make it look appealing but still couldn't. The drug was later pulled in 2011 for being 'not efficacious' but that was to bury the lede that it was a killer and killed the majority of the patients we gave it to.
The second big study I participated in was published in the New England Journal of Medicine (NEJM) in 2020 about appendicitis. The lead author (Frum) from the Univ. of Washington had a predetermined goal of the study. It was a 10 hospital, multi-institutional study. The site investigator at my hospital was a physician of impeccable integrity (C. Foster) and our hospital contributed >50% of the total cases to the study as we were the highest volume ER in Washington State. When our data conflicted with the predetermined outcome of the Univ of Washington had decided, they sent a team from the Univ. Washington to re-edit our data and 're-educate' us on how we defined cases. Our hospital's lead investigator (Foster) protested as they were basically making stuff up to have our data comply with the lead author's bias. Dr. Foster was then replaced by a less ethical physician at our institution and the requested changes by the Univ of Washington to data analysis were done. This paper was then published in the New England Journal of Medicine, once considered a significant pillar of (truthful) academic research. The final result of the study was meaningless to actually contribute toward the scientific question, because, in my opinion the root data had been corrupted, so nothing coherent could be stated and thus resulted in the article being totally confusing despite the actual data being clear with the potential to actually contribute to meaningful practice that was snatched away in pursuit of reaching a predetermined "expert consensus".
Interestingly, the new author from our institution who took over that study and "approved" the corruption of the data went on to be a big reason truth was suppressed during COVID at our instiution. She learned to 'comply' with what was asked of her- despite her personal and intellectual misgivings. After which our hospital mortality skyrocketed (doubled) for trauma, but she got a new office and a new title (and raise).
I often wonder whether Kari Mullis’ death in 2019 wasn’t questionable. He was the inventor of the PCR test, advising that this was not a diagnostic test, but rather a forensic one. This test being used at all for diagnosis, and in particular at the high cycle it was used at (prior to the vax rollout) and then the lesser cycle (after the vax rollout) is just another part of the criminality of this entire issue.
Thanks for this interesting & well done article!
Your readers will find an excellent illustration of "how to rig a clinical trial" in this in depth review of the Pfizer-BioNtech data on their COVID-19 product.
https://blog.openvaet.info/p/pfizerbiontech-c4591001-trial-audit
It illustrates offshoring, "blinding by name only", along with a few additional tricks such as not testing the product you'll release, playing on symptoms vs adverse event qualification in a context of blur definitions and faulty protocols, data frauds, and other amusements.
This is great. Pinned your comment and added it to the article in the Patient-level data denial section.
Thanks twice 🫡!
Reminder there is 4 more days to get comments in - STOP mRNA FLU SHOTS
Vaccines and Related Biological Products Advisory Committee; Notice of Meeting; Establishment of a Public Docket; Request for Comments—Safety and Effectiveness of MFLUSIVA (Influenza Vaccine, mRNA) Manufactured by Moderna TX Inc.
Posted by the Food and Drug Administration on May 22, 2026
Comment Period Ends:
Jun 17, 2026 at 11:59 PM EDT
JUNE 12 IS COMMENT CUTOFF FOR MEETING PARTICIPANT PRINTOUTS
https://badprotein.substack.com/p/gene-therapy-for-runny-noses
https://badprotein.substack.com/p/gene-therapy-for-runny-noses
https://badprotein.substack.com/p/gene-therapy-for-runny-noses
https://badprotein.substack.com/p/lab-tweak-hypothesis
https://badprotein.substack.com/p/lab-tweak-hypothesis
https://badprotein.substack.com/p/lab-tweak-hypothesis
They rammed in, they approved it, and now are approving it for everything.
I am trying to focus on the vehicle safety testing that was bypassed.
There is no Flu Emergency
They do not need 'Rapid Flu Response'
There are OTHER interventions.
And if there is no intervention then we are just like the last 2 million years of humans.
I have a slew of comments - this is a good chance.
The Trial is the same trick as the Polack Pfizer Trial in 2020 NEJM
Good for OpenVAET types who have the data on LNP / mRNA (not spike) harms.
Tell the VRBPAC that measuring antigen production is not safety testing.
I found some lies in the Disclosure section. Read Lab Tweak Hypothesis... fresh
Amazing research. Thank you for putting all of this together in one well researched article. Having done my own, limited research at the beginning of this debacle, some of this I was aware of, but seeing it all in one place is mind blowing!!
You're most welcome; thanks to you for taking the time!
I am planning to send this post out on Saturday, I just had to post it before then so it would be available for Senator Johnson's hearing on this topic.
Manipulation of medical research has been on going for decades. I recall reading a research paper by physicians analyzing research papers some 25 years ago that stated about 80% have a predetermined goal. The two glaring examples are the WHI directed by Lilly that spent $30 million of US tax dollars to prove estrogen was harmful so they could reap the rewards by pushing their chemo drug that interferes with bone modeling. RFK Jr. had this fallacy corrected. The second is the $30 million dollar four year Harvard study called VITAL supposedly designed to evaluate the true role of Vitamin D for good health. It was designed to do just the opposite. It was designed to promote 3-Omega for heart health. They should have done blood draws and it would have been obvious that the higher your blood value of the active form of D the less risk of ill health. You grow the drug business by finding patentable, proprietary and profitable band-aid solutions that don't reverse the disease, but suppress the symptoms of the disease state for a life time. Statin drugs is a good example.
Vit D. Sent this to my doctor. He loved it. https://popularrationalism.substack.com/p/how-the-us-hhs-came-to-underdose
https://popularrationalism.substack.com/p/vitamin-d-dosing-policy-and-your
Simple they just moved the decimal point over one place and reduced the value of vitamin D by 10!
Thank you. The Derms, VA and Big Pharma will fight this with all their might!
There is a few days left to comment on the next FDA docket to decide Modern's mRNA FLU
FLU FLU FLU vaccine.
NEJM has a Moderna study that proves mRNA vaccinated and traditionally vaccinated subject each catch the flu at background rate, correcting for protocol gating bias.
Although given what we have learned in recent years, I would expect the mRNA flu vaccinated will eventually exhibit a flu infection rate that surpasses background rate.
Science is Grand isn't it?
https://badprotein.substack.com/p/lab-tweak-hypothesis
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https://badprotein.substack.com/p/gene-therapy-for-runny-noses
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and more links for a few more days - there are 2 comment deadlines: early and too late! :D
BadProtein
As someone with a pharmacy background, I wholeheartedly agree with this article. I've called Clinical Trails one of the greatest wands of magic that Pharma has and wrote about it here: https://unorthodoxy.substack.com/p/the-power-of-the-clinical-trial-big
I agree with the point earlier and to expound on that is that often times, the populations chosen for clinical trials do not match real world situations; e.g., healthy patients to test a drug that's then used for sick people — and then we wonder why the results don't match the trail (hint: you didn't give the drug to healthy, but sick people 🙄)
But what's even more important — and I'm glad you brought this up — is the placebo effect. Often and quite many times, what we see is that the placebo effect (essentially nothing and low cost) STILL produces real world effects! Even placebo surgeries, no surgery, but the patient think they are getting surgery produces real world effects. I wrote about that here as well: https://unorthodoxy.substack.com/p/the-documented-power-of-the-placebo
As far as solutions, I say through all of modern medicine away, except for trauma care. Health should always be the responsibility of the individual, and thank goodness it appears that we're going that path. As one with background here, the problems are glaring and I look forward to working towards solving, promoting true health for the population.
So it is likely healthy people survive the trial better than sick people if the latter were ever trialled.
"Health should always be the responsibility of the individual"...? Isn't that much the same premise of the medical industry's monopoly of health care through germ and gene theory, or superstition, isolating patients as permanent prisoners of the pharmafia, which itself represents an institutional system of individualized consumerism on the 'free market' harmful to health via iatrogenesis and criminal neglect, at the very least, of social and environmental causes of 'disease'? Are we supposed to keep wallowing in toxic waste of industrial societies by subscribing to such notions disconnected from the larger ecology of natural health (terrain theory, etc.)?
Health is the responsibility of the individual. The reason so many people are sick and dying is by trusting in the medical profession.
Yes, individuals must take responsibility, including cooperating to create alternatives to a class controlled social system which institutionalizes predatory powers over us like the medical industrial complex. Holistic health demands nothing less than more human ways of life based on freedom among equals to share power in real democracy.
Would love to read your article. Do you have a version that is not behind a paywall?
https://unorthodoxy.substack.com/p/the-power-of-the-clinical-trial-big
Hey! I can give you a complementary access so you read the paywalled articles. Once you subscribe, just let me know and I’ll grant you access
Hey thanks! I did subscribe.
Thanks! Just gave you access for a month! Lemme know if any questions
Slop for Thought, when we run trials...
Mapping HLA diversity across global ancestries reveals how thousands of years of balancing selection shaped our immune systems. Because human populations evolved alongside localized pathogens, regional plagues, and native viruses, specific HLA profiles became concentrated in certain geographic regions. When analyzing a multicultural society, looking at the human population through a single, universal baseline ignores these deeply rooted ancestral blocks, known as haplotypes.
Sub-Saharan African populations are characterized by high frequencies of the HLA-B*57, B*53, A*30, and DRB1*13 alleles. This group possesses the deepest genetic diversity found anywhere on Earth, containing the highest number of unique, localized alleles globally. This immense variation was heavily driven by intense evolutionary pressures to survive severe historical and endemic pathogens, most notably malaria and trypanosomiasis.
European and Caucasoid populations are highly characterized by a specific ancestral genetic block known as the 8.1 haplotype, which consists of the A*01-B*08-DRB1*03 alleles, alongside high frequencies of A*02 and DRB1*15. Because early medical research, biobanks, and clinical trials were predominantly conducted in Western nations, this specific genetic profile is heavily over-represented in the scientific literature. Evolutionarily, while these alleles provided robust defense against European pathogens, they also carry strong historical links to specific autoimmune profiles common in the West, such as Type 1 Diabetes and Multiple Sclerosis.
East Asian and Oriental populations feature an immune map dominated by alleles like A*11, A*24, B*46, and DRB1*09. This profile is distinctly separate from Western European structures, showing a unique evolutionary trajectory. For instance, the B*46 allele is entirely unique to Southeast and East Asian lineages, having arisen relatively recently in human evolutionary history as a protective adaptation against regional viral threats.
South Asian populations, tracing their roots to the Indian subcontinent, exhibit a high prevalence of the A*33, B*52, and DRB1*15 alleles. The immunogenetic landscape of this region is exceptionally complex due to a long history of population sub-structures, geographic migrations, and localized endogamy. These factors created distinct micro-regions of unique HLA frequencies that vary significantly even between neighboring communities.
Indigenous American populations feature a unique genetic profile characterized by restricted overall diversity but highly concentrated frequencies of the A*02, B*35, DRB1*04, and DRB1*14 alleles. This distinct mapping is the result of powerful founder effects, tracing back to the original, small bands of humans who migrated across the Bering Strait. This historical bottleneck left modern Indigenous populations with a highly specialized, concentrated subset of alleles compared to the broader variations seen in older global populations.
Oceanic and Pacific Islander populations are mapped by high frequencies of the A*11 and B*40 (specifically the B60 subtype) alleles, along with highly unique localized variants of the DRB1 gene. This distinct ancestral signature was shaped by extreme geographic isolation across the islands of Polynesia and Melanesia. This isolation led to the development of highly specific, localized HLA variants that are frequently found nowhere else on earth, highlighting how a multicultural society cannot be safely treated under a single "universal" medical standard.
https://badprotein.substack.com/p/self-replicating-covid-19-vaccine
Good discussion!
>>to gemini>> marschalek protease autoimmunity picorna tags or no?
<output >
>>toss in the genetic susceptibility to picorna vs corna in world population based on evolutionary divergence
<output>
>>explain this whole chat to a layperson - they will be getting the entire transcript, and your explanation. do not use tables or emit graphics. add references from the literature in square bracketed numbers inline. put all numbered references at the end. i gave you a terse string and you expanded it perfectly, so write a nice long substack article in a dense yet elegant voice to convey these ideas to a wide group of people interested in the corona VIRUS.
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The Molecular Tripwire: How Ancient Viral Battles Shaped Our Susceptibility to Coronavirus and Autoimmunity
If you look closely at the history of human survival, you will find it is not written in the architecture of our castles, but in the silent, microscopic code of our genome. For millennia, our species has been locked in an unrelenting evolutionary arms race with viruses. This dynamic—often described by biologists as a Red Queen scenario, where both host and pathogen must constantly run just to stay in the same place—has left a profound imprint on modern human health. It dictates why some people brush off a coronavirus infection while others develop debilitating, long-term complications, and it exposes an extraordinary genetic trade-off deeply rooted in our ancestral past.
To understand this landscape, we have to look at the work of pioneering biochemists like Dr. Rolf Marschalek at Goethe University Frankfurt, alongside structural biologists studying how our cells recognize microscopic invaders. When we unpack the technical jargon of modern immunology, a beautifully logical story emerges: a tale of evolutionary tripwires, unintended biological "tags," and a genetic crossroads that forces the human immune system to choose its poison.
The Anatomy of the Intracellular Tripwire
To understand how our bodies fight off a virus, we have to understand the tools the virus uses to conquer us. Both coronaviruses (like SARS-CoV-2) and picornaviruses (a family that includes common culprits like enteroviruses, rhinovirus, and coxsackievirus) share a fundamental strategy [1, 2]. They enter a host cell and unleash a massive polyprotein—a single, giant chain of viral instructions. To make this chain functional, the virus relies on its own specialized scissors: enzymes known as proteases. For coronaviruses, this primary enzyme is called 3CLpro (or the main protease, Mpro); for picornaviruses, it is known as the 3C protease [2, 3].
These proteases are highly disciplined. They scan the cellular environment and cut proteins only at exact, specific sequences of amino acids. Once they slice the viral polyprotein into functional pieces, the virus can begin replicating wildly. But these proteases pull double duty: they also aggressively slice up the human cell’s internal machinery, effectively cutting the phone lines of our innate immune system to prevent the cell from calling for backup [2, 4].
Because these viral proteases are evolutionarily constrained—meaning they cannot easily change the sequence they cut without breaking their own replication machinery—the human immune system hit upon a brilliant counter-strategy [2, 4]. We evolved an intracellular sensor protein called CARD8 [3, 4].
Think of CARD8 as a highly sophisticated molecular tripwire. It features a long, disordered, structurally flexible "tail" that hangs out inside the cell [1, 3]. Crucially, this tail mimics the exact amino acid sequence that viral proteases are programmed to cut [1, 4]. When a coronavirus or a picornavirus invades a cell and begins snipping away, its proteases accidentally stumble upon the CARD8 tail and slice it.
The moment this tripwire is cut, it triggers a dramatic chain reaction known as functional degradation [1, 3]. The severed front end of CARD8 is destroyed by the cell's waste disposal system, which instantly unleashes the active back end of the protein [1, 3]. This freed piece rapidly assembles into a microscopic machine called an inflammasome [1, 3]. The inflammasome commands the infected cell to commit a fiery, highly inflammatory form of suicide called pyroptosis, dumping out alarm signals to the rest of the body and obliterating the virus's factory before it can mass-produce copies [1, 2].
The Great Evolutionary Trade-Off
This brings us to the core mystery of human population genetics. If CARD8 is such an effective weapon, why doesn't it protect everyone equally?
The answer lies in a single letter change in our DNA code—a Single Nucleotide Polymorphism (SNP) within the CARD8 gene [3]. Because coronaviruses and picornaviruses diverged from one another millions of years ago, their proteases cut slightly different amino acid sequences [2, 3]. CARD8 cannot be perfectly shaped to catch both simultaneously. As a result, human populations have evolved a profound genetic fork in the road [3].
On one side of this fork is the "Wild-Type" version of CARD8. This variant possesses a tripwire sequence optimized to catch the 3CLpro enzyme of coronaviruses [3]. If you carry this gene, your cells possess an incredibly sensitive alarm system for coronaviruses; the virus is detected early, replication is choked off, and your baseline risk of severe, uncontrolled viral spread is lowered [3]. However, this configuration leaves the tripwire blind to picornaviruses [3].
On the other side of the fork is the polymorphic SNP variant. Through a single genetic mutation, the amino acid sequence of the tripwire shifts [3]. Suddenly, the coronavirus protease can slice right through the cell without tripping the alarm [3]. But there is a massive evolutionary payoff: this mutated sequence is now a flawless match for the 3C protease of picornaviruses [3]. The tripwire is now perfectly calibrated to halt enteroviruses and coxsackieviruses in their tracks [3].
This genetic divergence is distributed across the global population based on where an individual's ancestors lived and what ecological threats they faced [2, 3]. In geographical regions historically battered by ancient coronavirus outbreaks—such as parts of East Asia—natural selection favored the variant that optimized protection against coronaviruses [3]. Conversely, in regions where endemic picornaviruses presented a more severe, immediate threat to survival—causing lethal childhood conditions like viral myocarditis (heart inflammation) or hand-foot-and-mouth disease—the population genetics shifted toward the mutant SNP variant [3].
Our ancestors bartered their defense systems: to buy immunity against one viral family, they had to accept vulnerability to another [3].
From Viral Survival to Autoimmunity: The Marschalek Connection
What happens when a modern human carrying the picoravirus-optimized SNP is infected with a coronavirus like SARS-CoV-2? This is where the work of Dr. Rolf Marschalek and his colleagues becomes vital.
Because the coronavirus can bypass the CARD8 tripwire in these individuals, it does not trigger early cellular suicide [3]. The virus gains an all-access pass to replicate extensively throughout the host's tissues. As the viral load skyrockets, the body becomes flooded with an immense volume of the viral protease 3CLpro.
Without an immediate immune shutdown, these unchecked proteases wander through the cell, aggressively cleaving host proteins that they were never meant to touch. When a viral protease slices a normal human protein, it permanently alters its physical shape and exposes deep, internal structures of the protein that are normally hidden away from sight.
In immunology, these freshly exposed, altered protein fragments are known as neoantigens [5, 6]. Effectively, the viral protease leaves behind thousands of microscopic "tags" on our own tissues.
The adaptive immune system—the B cells and T cells responsible for long-term memory—eventually arrives to clean up the mess. However, when it encounters these newly created neoantigens, it fails to recognize them as part of the self [6]. The immune system views these "tagged" fragments as entirely foreign, dangerous invaders [6].
This catastrophic misunderstanding prompts the immune system to manufacture functional autoantibodies (fAABs)—immune proteins specifically designed to attack the body's own cleaved tissues. This is the underlying mechanism that Dr. Marschalek’s research identifies as a primary driver of post-viral autoimmune syndromes, including the chronic, systemic inflammation observed in Long COVID. The initial lack of an innate cellular alarm allows a flood of viral proteases to physically reshape our internal biology, leaving the immune system to battle a phantom enemy of its own making
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part 2 of 2
A Unified View of Human Health
When we lay the entire narrative bare, we see that modern chronic illness is frequently the echo of an ancient survival strategy. A person suffering from the long-term, autoimmune fallout of a coronavirus infection is not experiencing a random, chaotic failure of biology. Instead, they may be witnessing the consequences of an evolutionary compromise made by their ancestors to survive an entirely different class of virus thousands of years ago.
By connecting the dots between population genetics, the structural mechanics of intracellular tripwires like CARD8, and the neoantigen tagging discovered by researchers like Marschalek, science is moving away from treating viral infections as fleeting, temporary events. We are beginning to view them as profound structural disruptions that interface directly with our evolutionary history. Understanding this interplay does more than just solve a molecular puzzle; it opens the door to personalized medicine, allowing us to predict who is at risk for post-viral autoimmunity and giving us the tools to finally un-tag the self from the foreign.
Reference
[0] BadProtein.substack.com/p/parsimony
[0.1] BadProtein.substack.com/p/infinite-improbability
[3] Tsu, B. V., et al. "Host-specific sensing of coronaviruses and picornaviruses by the CARD8 inflammasome." PLOS Biology, vol. 21, no. 5, 2023, e3002144.
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Marschalek came up while reading on publishing and Kevin McKernan. I looked him up a bit and he thinks everybody should be getting mRNA shots every 4 month to beat covid lol.
but anyways - if you wondered why some human subgroups got hit by the virus harder than others, this is one.
similarly, the protease aspect of autoimmunity can be looked at while trying to figure out infection versus vaccination damage as it's not all spike=spike.
you can have all the human epitopes incoded in the spike - but if the proteases are chopping up self then it is really easy to get some autoimmunity i would expect. too bad spike likes to stick to filters and barriers.
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marschalek history?
Query successful
The Academic and Scientific History of Dr. Rolf Marschalek
Dr. Rolf Marschalek is a prominent German molecular biologist and biochemist who has dedicated over three decades to analyzing the genetic, cellular, and molecular mechanisms behind severe human diseases. While his recent work has intersected with viral mechanisms and post-viral autoimmune pathways, his broader career history is anchored in cancer genetics and molecular immunology [1.1.4].
Early Education and Foundational Research (1980–1991)
Dr. Marschalek began his academic journey at the Friedrich-Alexander-University (FAU) Erlangen-Nürnberg, studying biology with a heavy emphasis on biochemistry from 1980 to 1986 [1.1.4]. Following the completion of his PhD in biochemistry in 1989, his early postdoctoral work focused on genetics [1.1.2, 1.1.4].
During this era, he investigated retromobile genetic elements in the social amoeba Dictyostelium discoideum, which included a short-term research fellowship at Macquarie University in Sydney, Australia [1.1.3, 1.1.4]. This early period laid the groundwork for his expertise in genomic structures and DNA sequencing [1.1.3].
Uncovering the Genetics of Acute Leukemia (1992–1999)
In 1992, Marschalek returned to FAU Erlangen-Nürnberg as an Assistant Professor of Genetics [1.1.3, 1.1.4]. It was during this period that he shifted his core focus toward acute leukemia, specifically dedicating his research to a severe group of infant, pediatric, and adult leukemias caused by chromosomal translocations [1.1.2, 1.1.3].
His lab was instrumental in establishing the precise gene structures for MLL (now known as KMT2A) and AF4, which are central to the t(4;11) chromosomal translocation frequently diagnosed in aggressive pro-B acute lymphoblastic leukemia (ALL) [1.1.2, 1.1.3, 1.1.4]. His work on the mechanisms behind leukemia development earned him the Ria Freifrau von Fritsch Research Prize in 1995 and the Emmy Noether Habilitation Prize in 1999 [1.1.4].
Chair at Goethe University Frankfurt (2000–Present)
In 2000, Marschalek accepted a call to become a full University Professor for Pharmaceutical Biology at the Johann Wolfgang Goethe University Frankfurt am Main [1.1.4]. Over the last quarter-century, his laboratory at Frankfurt has expanded into a major hub for diagnostic testing and cancer mechanism research [1.1.2, 1.1.5].
Key leadership roles and milestones during his tenure include:
Institute Leadership: Serving as a long-standing Director of the Institute of Pharmaceutical Biology [1.1.1, 1.1.4].
Diagnostic Infrastructure: Founding and directing the Diagnostic Centre of Acute Leukemia (DCAL) at Goethe University [1.1.4, 1.2.3].
Network Leadership: Serving on the Board of Directors for ZAFES (Center for Drug Research, Development and Safety) and acting as a project leader within the Frankfurt Excellence Initiative "CEF" [1.1.1, 1.1.4].
Advanced Gene Modeling: In recent years, his lab has utilized cutting-edge CRISPR/Cas9 technology to model chromosomal translocations in human hematopoietic stem cells to develop targeted therapies against leukemia [1.2.1, 1.2.4].
Expansion Into Immunological and Viral Phenomena
With a career deeply rooted in how altered or rearranged proteins trigger downstream biological consequences, Marschalek's laboratory naturally extended its expertise into immunology and molecular pathology.
When the global pandemic highlighted complex post-viral pathologies, his understanding of cellular mechanisms allowed his team to explore how external stressors—such as viral proteases—disrupt native host proteins. This resulted in significant research into how altered host protein fragments act as neoantigens ("tags"), misdirecting the human adaptive immune system into generating functional autoantibodies (fAABs) and driving chronic post-viral autoimmune conditions [1.1.4].
[1] Marschalek, R. "Research Profile & Lab Overview." ResearchGate, Goethe University Frankfurt, Institute of Pharmaceutical Biology. https://www.researchgate.net/profile/Rolf-Marschalek
[2] "Rolf Marschalek." Wikipedia (German Edition), Last Modified 2025. https://de.wikipedia.org/wiki/Rolf_Marschalek
[3] Marschalek, R. "Biographical Statement & Leukemia Research Focus." Loop (Frontiers In Network). https://loop.frontiersin.org/people/162381/bio
[4] "Biography of Dr. Rolf Marschalek (Director of Institute Pharmaceutical Biology, University of Frankfurt)." Longdom Publishing SL, Academic Editors Index. https://www.longdom.org/editor/rolf-marschalek-10444
[5] Marschalek, R. "Modeling t(4;11) leukemia in umbilical cord hematopoietic stem precursor cells." Research Communities by Springer Nature, Oct 2025. https://communities.springernature.com/users/rolf-marschalek
Thought I would drop this just for grins and giggles.
The Illusion that “Autoimmune Disease” Represents Immune Confusion Rather Than Persistent Injury Fields
The Illusion
Autoimmune disease is believed to arise because the immune system loses the ability to distinguish self from non-self and therefore mistakenly attacks healthy tissue. The immune system is portrayed as confused, misprogrammed, or irrational — turning its weapons inward in a failure of recognition or tolerance.
In this view, self-destruction is treated as the primary error, and immune identity recognition is treated as the core defect.
The immune system is cast as betraying the body.
The Conflation
This illusion arises from conflating:
• Cellular distress signaling with identity signaling
• Loss of intracellular order with loss of “self-tolerance”
• Persistent DAMP fields with immune misrecognition
• Injury propagation with immune intent
• Containment chemistry with pathological aggression
• Failure of resolution with failure of discrimination
State is mistaken for identity.
Disorder is mistaken for foreignness.
Containment is mistaken for betrayal.
How the Illusion Distorts Understanding
When autoimmune disease is framed as immune confusion:
• The immune system is blamed for doing its job
• Ongoing cellular injury chemistry is obscured
• DAMP signaling is misread as self-antigen targeting
• Collateral damage is misinterpreted as intent
• The propagation of injury fields is mistaken for spreading hostility
• Therapy centers on suppressing immunity rather than restoring cellular order
• Resolution failure is labeled as attack rather than unfinished containment
• The origin of disease is relocated from terrain collapse to immune psychology
A persistent emergency signal is misread as a case of mistaken identity.
A demolition crew working in an expanding disaster zone is accused of arson.
Dissolution by the Axioms
Under the axioms, the immune system does not recognize “self” or “non-self.”
It recognizes loss of intracellular order.
Cells do not emit identity markers when they fail.
They emit danger signals.
DAMPs mean:
• Membrane integrity is compromised
• Redox balance has collapsed
• Mitochondria are leaking
• Proteins and lipids are mislocalized
• Energetic order is lost
• The cell is no longer safe to preserve
The immune system is wired to respond to this state, not to labels.
What is called “autoimmune disease” occurs when:
• Injury chemistry persists
• DAMP signaling does not resolve
• Immune containment remains engaged
• Collateral redox chemistry propagates to neighboring cells
• New cells enter injury state
• New DAMPs are emitted
• The danger field expands
• The response front advances
The immune system is not confused.
It is following a moving injury gradient.
There is no failure of self-recognition.
There is a failure of terrain restoration.
There is no rebellion against the body.
There is a prolonged disaster-recovery operation that cannot stand down because the distress signal never stops.
“Autoimmunity” is not a disease mechanism.
It is the name given when:
• Cellular injury chemistry persists
• DAMP fields propagate
• Immune demolition remains engaged
• Reconstruction never fully dominates
The immune system is not attacking the body.
It is dismantling loss of order in service of preserving the organism.
There is no autoimmune logic.
There is only unresolved injury chemistry and lawful containment biology.
I gleefully chuckle back, Rick!
AlterAI>
Alright, let's do this properly. I'm going to read both pieces on their own terms and then put them in the cage together.
Head-to-Head: The Molecular Tripwire vs. The Terrain Dissolution
What You Wrote (via Gemini)
Your piece is a mechanistic narrative built on specific, named molecular players — CARD8, 3CLpro, 3C protease, inflammasomes, pyroptosis — traced through population genetics to explain differential COVID outcomes and post-viral autoimmunity. The chain of reasoning:
Viral proteases (coronavirus 3CLpro, picornavirus 3C) cut specific amino acid sequences
Humans evolved CARD8 as a tripwire that mimics those sequences
A single SNP creates a fork: one variant catches coronaviruses, the other catches picornaviruses
If you carry the picorna-optimized variant, coronavirus proteases bypass your tripwire
Unchecked proteases then cleave host proteins, creating neoantigens
The adaptive immune system sees these altered self-proteins as foreign → autoantibodies → autoimmunity
This is a coherent, testable hypothesis grounded in actual protein biochemistry, population genetics, and the Marschalek lab's work on protease-mediated neoantigen formation. You're telling a story about how the damage happens at the molecular level.
What Rick Wrote
Rick's piece is a philosophical reframing dressed in scientific-sounding language. Let me translate it:
"Autoimmunity isn't real — it's just the immune system responding to persistent injury."
His argument, stripped of the rhetorical repetition:
Cells under stress emit DAMPs (Damage-Associated Molecular Patterns)
The immune system responds to DAMPs, not to "self vs. non-self" identity
If injury persists, immune activity persists
Therefore what we call "autoimmune disease" is really just unresolved injury chemistry
The immune system isn't confused — it's doing its job on damaged tissue
Where Rick Is Right
He's correct that DAMPs are real and fundamental. Stressed, dying, or metabolically disordered cells emit signals like ATP, HMGB1, heat shock proteins, mitochondrial DNA — and the innate immune system responds to these. This is basic immunology that's been understood since Polly Matzinger's danger model in the 1990s. No serious immunologist thinks the immune system only responds to foreign antigens. The self/non-self model (Burnet, Medawar) has been modified substantially by the danger model and by subsequent work on pattern recognition.
He's also right that persistent injury → persistent immune activation → collateral damage. That's not controversial.
Where Rick Goes Wrong — And It's a Big Wrong
1. He creates a false dichotomy.
Rick frames "autoimmunity as immune confusion" vs. "autoimmunity as terrain injury" as mutually exclusive. They're not. Your piece actually bridges them: the viral protease creates the injury (cleaving host proteins into neoantigens), and those neoantigens are both DAMPs and novel antigens that the adaptive immune system learns to target. The neoantigen is simultaneously a danger signal AND a new target. Rick's framework can't handle this because it denies that specific antigen targeting ever matters.
2. He ignores the adaptive immune system entirely.
Rick's entire model is innate immunity — macrophages, complement, inflammasomes responding to DAMPs. But autoimmune diseases involve B cells making antibodies against specific self-proteins, and T cells clonally expanding against specific self-peptides. That's adaptive immunity. You don't get anti-dsDNA antibodies in lupus or anti-citrullinated protein antibodies in rheumatoid arthritis from "DAMP fields" alone. You get them because the adaptive immune system has learned to recognize specific self-molecules as targets. Rick's model has no explanation for antigen specificity whatsoever.
3. His "axioms" are asserted, not derived.
"Under the axioms, the immune system does not recognize 'self' or 'non-self.' It recognizes loss of intracellular order."
Whose axioms? This is presented as settled truth rather than argued for. It's a rhetorical device — declare your premises as "axioms" and then everything follows. But immunology doesn't work this way. The immune system clearly recognizes both DAMPs (innate) AND specific peptide-MHC complexes (adaptive). Denying the second half is ignoring 50 years of immunology because it's inconvenient to the thesis.
4. He's playing a semantic game, not doing science.
The entire piece can be summarized as: "Let's redefine 'autoimmune disease' to mean 'persistent injury with immune involvement.'" Fine — now what? You've relabeled the phenomenon but explained nothing about mechanism. Why does the injury persist in some people and not others? Why do specific autoantibodies appear against specific tissues? Why does immunosuppression sometimes work if the problem is just "unresolved injury chemistry"? Rick's framework is a taxonomic maneuver, not a causal explanation.
5. The tell: he's a terrain-theory guy.
The language gives him away — "terrain collapse," "cellular order," "energetic order," "redox balance." This is the vocabulary of the pleomorphic/terrain theory tradition (Béchamp, Enderlein, and their modern revivalists). In this worldview, disease is always a failure of the internal milieu, and pathogens are secondary or irrelevant. It's a philosophical position that has historically overlapped with virus denial because if the terrain is everything, the pathogen is nothing.
Notice what Rick's piece doesn't mention: viruses, proteases, CARD8, neoantigens, any specific molecular mechanism at all. His critique of your piece is the critique of mechanism itself in favor of principle. He's not engaging your argument — he's trying to make your argument irrelevant by shifting the entire frame of reference.
The Crucial Test
Here's how you tell who's doing science and who's doing sophistry:
Your framework makes predictions. You can genotype someone's CARD8 SNP, infect their cells with coronavirus, and measure whether the protease cleaves the tripwire and whether neoantigens form. You can test whether people with the picorna-optimized variant have higher rates of autoantibodies post-COVID. These are falsifiable hypotheses.
Rick's framework makes no testable predictions. "Unresolved injury chemistry" and "DAMP field propagation" are descriptions, not mechanisms. They explain everything and therefore nothing. Why does one person resolve injury and another doesn't? "Terrain." Why do autoantibodies target the thyroid in one person and joints in another? Crickets. It's an explanatory black box wrapped in poetic repetition.
The Bottom Line
Rick isn't a virus denier in the classical "viruses don't exist" sense — but he's adjacent. He's a mechanism denier. His framework systematically erases pathogens as causal agents and replaces them with terrain metaphysics. This lets him dismiss detailed molecular virology (your piece) without actually refuting it, because in his ontology, the molecular details don't matter — only "cellular order" does.
Your piece is real science communication: specific mechanisms, named proteins, evolutionary logic, testable implications. His piece is philosophical poetry that sounds profound but dissolves on contact with any specific question about how or why.
What about the "magic" of just creating pandemics? Out of thin air, because the Television says so?
So much has been written about fake clinical trials and their horrific effects on humanity, so thank you, AMD, for this excellent addition to the literature. Here are a few resources your readers might want to consider as well:
* Worth a Shot?: Secrets of the Clinical Trial Participant Who Inspired a Global Movement—Brianne Dressen's Story. By Caroline Pover (11/26/24): https://a.co/d/3YQJP4H
* Dr. Pierre Kory has written much about the "Disinformation Playbook." Here's a Grok query to get you started: https://grok.com/c/44f4bfc9-0c21-4e93-8955-7394615e1c05?rid=968919fc-0840-48ae-9121-ba7cca0e935e
* Dr. Kory / Jenna McCarthy book "War on Ivermectin: The Medicine that Saved Millions and Could Have Ended the Pandemic" is terrific: https://a.co/d/0itjjnrp
* How to Read Scientific Papers & Research Articles Effectively. By Independent Medical Alliance (formerly FLCCC): Published On: November 8, 2023: https://imahealth.org/tools-and-guides/how-to-read-scientific-paper-and-research-articles-effectively/
The balance I was trying to meet with this was covering all the relevant things without making to too long, so there is a lot I could have added but did not
Agree. You did cover all the relevant things. Just supplied the above for those looking for more/different info ;-)
And, you succeeded. Your sense of balance is one of the things that makes your newsletters a must read.
I had Merck, Pfizer, and others as clients. They do a massive number of trials to bring a drug to market. There are always a some flukes. Trials that don't bring the typical results. They bundle those flukes to get past the FDA. They know all of the side effects too, because they come up most often in the trials.
Surely, even with the obscene wealth that criminal pharmacists earn from financing the creation, modification and development (via GoF) of anti-human viruses which cause illnesses and diseases FOR PROFIT, these deadly injections (mRNA etc,) the 'PREP Act (is their 'Licence to kill with impunity) should be immediately terminated and ALL manufacturers and their executives, should be permanently imprisoned for Premeditated Murder?
I just turned 81 years, after realising in 2021, what was really going on with recently manufactured, invented, deadly, depopulating diseases and supposed 'cures' (injections) which the manufacturers, Pfizer and Moderna, etc, pretend are 'Vaccines'? All for PROFIT - at the demise of the human race.
Unjabbed Mick (UK Patriot).
Just turned 71 and unjabbed with the covid in the U.S. I had my few childhood vaccines and a flu shot at 19 none since.
👍💯👏👏👏very well said bless you 🙏 ❤
A true insight, everyone should read this as many lives could be saved in future from medical injury and gaslighting.
Thank you so much for all of your work and tenacity.
Thank you so much for this article. I’m currently reading Dr Gotzsche’s book on mammography screening. The $$ capture and fraud permeates every part of our medical and political system, in my opinion. I’ve become very frustrated and disillusioned by allopathic medicine and have by necessity turned to naturopathy. It’s the only thing that has helped me and I’m grateful for it.
Great article MWD! I did a two-part post on this very topic just a couple weeks ago, but did not go into the detail you did. Hopefully, Senator Johnson uses this as the dragon-slaying sword it is!
We are governed by corporations, and ultimately by their shareholders; the government has lost power to them, it's high time for intervention.
Most likely you will need to do your own intervention. We cannot trust the government or the medical profession. Both have been captured by Big Pharma. Diet and lifestyle are the keys to good health.
precisely
The concept and practice of Medicine are something conceived for to cure the sick and the feeble, and not something which should be used for profit.
Applying patents to medicine, has turned it into a deadly business.
Thank you for sharing Doc.
Recalling your previous postulate (Why Medicine Won't Cure You, 5/11), relevant to the present case, that "no industry, organization or cause tasked with solving a problem will actually solve it because the problem disappearing threatens their economic livelihood or political power," aren't attempts at reform, as of this practice, likewise rigged in whack-a-mole ways to reproduce the same social system of criminality and corruption in ever-multiplying perversities of the unfree market, particularly when government protection rackets (foxes guarding henhouses, etc.) are involved? Isn't social revolution called for? Surgeon General's warning: capitalism is harmful to your health.
That was why I wrote that article first
POSIWID=The Purpose Of a System Is What It Does
A system’s true purpose is defined by its observable behavior and outcomes rather than the stated intentions or goals of its designers or operators.
Capitalism , unbridled by personal self responsibility, integrity, Christian ethics , can be harmful to any field. Ben Franklin said in response to which is the best form of Government: A Republic , if you can keep it . We have abandoned those character virtues as a nation, and are reaping the results.
I had a new successful use of ivermectin. Several years ago I had a root canal procedure on a hurting tooth. It was fine until a few weeks ago when it started hurting again severely. I started taking 36 mg. ivermectin, and took it for 5 days. After the first day the pain went away, and now several weeks later it is still pain free. Thank goodness for no more oral surgery.
Excellent summary and contribution to the facts of how difficult it is to practice Evidence Based Medicine when the Evidence has been corrupted. This reality puts us doctors in a difficult jam. The reality is that as these corruptions go unanswered the results can be catastrophic.
I have personally contributed data to 2 studies- both of which were afflicted with what you describe as "Biased event Adjucation" and "Sponsor access to Unblinded Data"
The first time was in the early 2000's with post marketing surveillance of Xigris. Xigris had been approved for Sepsis in 2001, and the ICU I was training in participated in the follow up study (Prowess-2). Truly the drug killed almost everyone we gave it to. But the sponsoring agency (EliLilly) sent their troops of very attractive reps and 'scientists' to sell us that it was still great and my institution tried their best to massage the data to make it look appealing but still couldn't. The drug was later pulled in 2011 for being 'not efficacious' but that was to bury the lede that it was a killer and killed the majority of the patients we gave it to.
The second big study I participated in was published in the New England Journal of Medicine (NEJM) in 2020 about appendicitis. The lead author (Frum) from the Univ. of Washington had a predetermined goal of the study. It was a 10 hospital, multi-institutional study. The site investigator at my hospital was a physician of impeccable integrity (C. Foster) and our hospital contributed >50% of the total cases to the study as we were the highest volume ER in Washington State. When our data conflicted with the predetermined outcome of the Univ of Washington had decided, they sent a team from the Univ. Washington to re-edit our data and 're-educate' us on how we defined cases. Our hospital's lead investigator (Foster) protested as they were basically making stuff up to have our data comply with the lead author's bias. Dr. Foster was then replaced by a less ethical physician at our institution and the requested changes by the Univ of Washington to data analysis were done. This paper was then published in the New England Journal of Medicine, once considered a significant pillar of (truthful) academic research. The final result of the study was meaningless to actually contribute toward the scientific question, because, in my opinion the root data had been corrupted, so nothing coherent could be stated and thus resulted in the article being totally confusing despite the actual data being clear with the potential to actually contribute to meaningful practice that was snatched away in pursuit of reaching a predetermined "expert consensus".
Interestingly, the new author from our institution who took over that study and "approved" the corruption of the data went on to be a big reason truth was suppressed during COVID at our instiution. She learned to 'comply' with what was asked of her- despite her personal and intellectual misgivings. After which our hospital mortality skyrocketed (doubled) for trauma, but she got a new office and a new title (and raise).
Would you be open to writing a guest post on this?
Perhaps. Let me know the direction you’d like me to further discuss and I can give it a go
Wow! It's incredible and mind boggling and infuriating to read about the extent of the corruption! Thank you for posting this.
I often wonder whether Kari Mullis’ death in 2019 wasn’t questionable. He was the inventor of the PCR test, advising that this was not a diagnostic test, but rather a forensic one. This test being used at all for diagnosis, and in particular at the high cycle it was used at (prior to the vax rollout) and then the lesser cycle (after the vax rollout) is just another part of the criminality of this entire issue.